Anesthetic Influence on Splanchnic Circulation

1988年4月至1991年3月，我们用肝动脉结扎的Beagle动物模型，观察了PaCO_2变化对内脏循环的影响，挥发性麻醉剂(氟烷、异氟烷和七氟醚)对肝脏循环和功能的影响，以及钙通道阻滞剂对肝细胞的保护作用。研究结果总结如下：1.低碳酸血症导致肝动脉血流量减少，但不影响体循环。高碳酸血症时门脉血流量和总肝血流量明显增加。结论：1.尽管肝脏总血流量增加，但高碳酸血症时吲哚青绿(ICG)的半衰期和血浆ICG清除量均小于低碳酸血症时，提示高碳酸血症时肝功能受抑。我们比较了在肝脏边缘供氧条件下，挥发性麻醉药对肝脏循环和功能的影响。用等浓度氟烷、异氟醚和七氟醚(1.5MAC)对9只结扎肝动脉的Beagle犬进行麻醉。氟烷和七氟烷的肝脏摄氧量有显著差异。与氟烷和异氟烷相比，七氟醚的供氧/摄氧比较小，同时保留了肝功能。低氧120min复氧可加重肝细胞损伤，引起肝血管痉挛。这种血管痉挛可能是由钙诱导的血管痉挛引起的，因为尼卡地平可以预防这种痉挛。提示尼卡地平的保护作用可能与其减轻血管痉挛有关。

With Grand-in-Aid for Scientific Research from the Ministry of Education, Science and Culture we investigated 1. the effects of alterations in PaCO_2 on splanchnic circulation, 2. the effects of volatile anesthetics (halothane, isoflurane and sevoflurane) on hepatic circulation and function in the beagle with hepatic artery ligation, and 3. the protective effects of a calcium channel blocker on the hepatocytes by using the isolated perfused rat liver model between April 1988 and March 1991. The results of the project are summarized as follows :1. Hypocapnia caused a decrease in hepatic arterial blood flow without affecting the systemic circulation. There was a significant increase in portal and total hepatic blood flows during hypercapnia. Despite the increase in total hepatic blood flow the half-life of indocyanine green (ICG) and plasma ICG clearance was less during hypercapnia than during hypocapnia, suggesting the depressed hepatic function during hypercapnia.2. We compare the effects of volatile anesthetics on hepatic circulation and function under condition of marginal hepatic oxygen supply. Equi-anesthetic concentrations (1.5 MAC) of halothane, isoflurane, and sevoflurane were administered to nine beagles with ligation of the hepatic artery. There was a significant difference in hepatic oxygen uptake between halothane and sevoflurane. Sevoflurane is accompanied by a smaller oxygen supply/uptake ratio than halothane and isoflurane, while it preserves the hepatic function.3. Reoxygenation after 120 min hypoxia aggravated the hepatocellular injury and elicited vasospasm of the liver. The vasospasm might be due to calcium-induced vasospasm, because it was prevented by nicardipine pretreatment. It was concluded that the protective effects of nicardipine may be related with attenuation of the vasospasm.